Premium
Low doses of corticosterone act in the dorsal hindbrain to enhance the arterial pressure response to both acute and repeated stress
Author(s) -
Looney Benjamin M,
Daubert Daisy L,
Su Ye,
Scheuer Deborah A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1171.4
Subject(s) - corticosterone , mean arterial pressure , heart rate , medicine , anesthesia , chronic stress , blood pressure , fight or flight response , dorsum , chemistry , hormone , anatomy , biochemistry , gene
We have shown that chronic treatment of the dorsal hindbrain (DHB) with 100% corticosterone (Cort) pellets enhances the mean arterial pressure (MAP) response to acute stress. The current experiments were performed to determine the effect of lower doses of Cort on the arterial pressure and heart rate responses to acute and repeated stress. Experiments were performed on male Sprague‐Dawley rats implanted with DHB Sham, 10%, 50% or 100% Cort pellets, n=4–6 per group. MAP and heart rate were measured via radiotelemetry (Data Science International). Rats were subjected to 1 h of restraint stress on days 6, 13, 14 and 15 days post pellet implantation. All doses of Cort significantly enhanced (P<0.05) the integrated MAP response to both acute and repeated stress relative to sham treatment. For example, on day 6 DHB sham, 10, 50 and 100% Cort treatment increased arterial pressure by 1509±496, 2736±193, 2737±499 and 2471±412 mmHg/60 min respectively, and on day 14 by 1959±328, 2952±414, 2435±301 and 2612±301 mmHg/60 min respectively. There were no significant differences (P=0.08) in baseline MAP between groups, but the 10% dose increased MAP from 103±3 on day 6 to 109±4 mmHg on day 15 (P<0.05). There were no significant effects of DHB treatment on baseline HR or the integrated HR response to stress. We conclude that even low doses of Cort enhance the arterial pressure response to acute and chronic stress. Funded by NIH grant # HL 076807.